Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle: A randomized clinical study

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Standard

Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle : A randomized clinical study. / Voss, Thomas S; Vendelbo, Mikkel H; Kampmann, Ulla; Hingst, Janne Rasmuss; Wojtaszewski, Jørgen; Svart, Mads V; Møller, Niels; Jessen, Niels.

I: Diabetes, Bind 66, Nr. 9, 2017, s. 2483-2494.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Voss, TS, Vendelbo, MH, Kampmann, U, Hingst, JR, Wojtaszewski, J, Svart, MV, Møller, N & Jessen, N 2017, 'Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle: A randomized clinical study', Diabetes, bind 66, nr. 9, s. 2483-2494. https://doi.org/10.2337/db16-1559

APA

Voss, T. S., Vendelbo, M. H., Kampmann, U., Hingst, J. R., Wojtaszewski, J., Svart, M. V., ... Jessen, N. (2017). Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle: A randomized clinical study. Diabetes, 66(9), 2483-2494. https://doi.org/10.2337/db16-1559

Vancouver

Voss TS, Vendelbo MH, Kampmann U, Hingst JR, Wojtaszewski J, Svart MV o.a. Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle: A randomized clinical study. Diabetes. 2017;66(9):2483-2494. https://doi.org/10.2337/db16-1559

Author

Voss, Thomas S ; Vendelbo, Mikkel H ; Kampmann, Ulla ; Hingst, Janne Rasmuss ; Wojtaszewski, Jørgen ; Svart, Mads V ; Møller, Niels ; Jessen, Niels. / Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle : A randomized clinical study. I: Diabetes. 2017 ; Bind 66, Nr. 9. s. 2483-2494.

Bibtex

@article{3b507cb5e15941d3a1aef327fa1fd7bc,
title = "Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle: A randomized clinical study",
abstract = "Hypoglycemia is the leading limiting factor in glycemic management of insulin-treated diabetes. Skeletal muscle is the predominant site of insulin-mediated glucose disposal and our study was designed to test to what extent insulin induced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycemia counter-regulation modulates insulin and catecholamine signaling and glycogen synthase activity in skeletal muscle.Nine healthy volunteers were examined on three randomized study days in a crossover design: i) hyperinsulinemic hypoglycemia (bolus insulin), ii) hyperinsulinemic euglycemia (bolus insulin and glucose infusion) and iii) saline control with skeletal muscle biopsies taken just before, 30 min and 75 min after insulin/saline injection.During hypoglycemia glucose levels reached a nadir of ∼2.0mmol/l and epinephrine rose to ∼900pg/ml.Insulin stimulated glucose disposal and glucose clearance in skeletal muscle were impaired whereas insulin signaling to glucose transport was unaffected by hypoglycemia. Insulin-stimulated glycogen synthase activity was completely ablated during hyperinsulinemic hypoglycemia and catecholamine signaling via PKA as well as phosphorylation of inhibiting sites on glycogen synthase all increased.",
keywords = "Journal Article",
author = "Voss, {Thomas S} and Vendelbo, {Mikkel H} and Ulla Kampmann and Hingst, {Janne Rasmuss} and J{\o}rgen Wojtaszewski and Svart, {Mads V} and Niels M{\o}ller and Niels Jessen",
note = "CURIS 2017 NEXS 229",
year = "2017",
doi = "10.2337/db16-1559",
language = "English",
volume = "66",
pages = "2483--2494",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "9",

}

RIS

TY - JOUR

T1 - Acute hypoglycemia in healthy humans impairs insulin stimulated glucose uptake and glycogen synthase in skeletal muscle

T2 - A randomized clinical study

AU - Voss, Thomas S

AU - Vendelbo, Mikkel H

AU - Kampmann, Ulla

AU - Hingst, Janne Rasmuss

AU - Wojtaszewski, Jørgen

AU - Svart, Mads V

AU - Møller, Niels

AU - Jessen, Niels

N1 - CURIS 2017 NEXS 229

PY - 2017

Y1 - 2017

N2 - Hypoglycemia is the leading limiting factor in glycemic management of insulin-treated diabetes. Skeletal muscle is the predominant site of insulin-mediated glucose disposal and our study was designed to test to what extent insulin induced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycemia counter-regulation modulates insulin and catecholamine signaling and glycogen synthase activity in skeletal muscle.Nine healthy volunteers were examined on three randomized study days in a crossover design: i) hyperinsulinemic hypoglycemia (bolus insulin), ii) hyperinsulinemic euglycemia (bolus insulin and glucose infusion) and iii) saline control with skeletal muscle biopsies taken just before, 30 min and 75 min after insulin/saline injection.During hypoglycemia glucose levels reached a nadir of ∼2.0mmol/l and epinephrine rose to ∼900pg/ml.Insulin stimulated glucose disposal and glucose clearance in skeletal muscle were impaired whereas insulin signaling to glucose transport was unaffected by hypoglycemia. Insulin-stimulated glycogen synthase activity was completely ablated during hyperinsulinemic hypoglycemia and catecholamine signaling via PKA as well as phosphorylation of inhibiting sites on glycogen synthase all increased.

AB - Hypoglycemia is the leading limiting factor in glycemic management of insulin-treated diabetes. Skeletal muscle is the predominant site of insulin-mediated glucose disposal and our study was designed to test to what extent insulin induced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycemia counter-regulation modulates insulin and catecholamine signaling and glycogen synthase activity in skeletal muscle.Nine healthy volunteers were examined on three randomized study days in a crossover design: i) hyperinsulinemic hypoglycemia (bolus insulin), ii) hyperinsulinemic euglycemia (bolus insulin and glucose infusion) and iii) saline control with skeletal muscle biopsies taken just before, 30 min and 75 min after insulin/saline injection.During hypoglycemia glucose levels reached a nadir of ∼2.0mmol/l and epinephrine rose to ∼900pg/ml.Insulin stimulated glucose disposal and glucose clearance in skeletal muscle were impaired whereas insulin signaling to glucose transport was unaffected by hypoglycemia. Insulin-stimulated glycogen synthase activity was completely ablated during hyperinsulinemic hypoglycemia and catecholamine signaling via PKA as well as phosphorylation of inhibiting sites on glycogen synthase all increased.

KW - Journal Article

U2 - 10.2337/db16-1559

DO - 10.2337/db16-1559

M3 - Journal article

C2 - 28596236

VL - 66

SP - 2483

EP - 2494

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 9

ER -

ID: 179366280